Treatment of Overt Hepatic Encephalopathy.

Norman L Sussman

Journal: Clinics in liver disease 2016;19(3):551-63

PMID: 26195208

Full Text on Elsevier Science View on PubMed

Abstract

Hepatic encephalopathy (HE) is defined by an altered mental status in the setting of portosystemic shunting, with or without cirrhosis. The basis of HE is probably multi-factorial, but increased ammonia delivery to the brain is thought to play a pivotal role. Medical therapies have typically focused on reducing blood ammonia concentrations. These measures are moderately effective, but further improvements will require identification of new therapeutic targets. Two medications, lactulose and rifaximin, are currently approved for the treatment of HE in the USA - new compounds are available off-label, and are in clinical trials. The presence of HE is associated with a higher risk of death in cirrhotic patients. Liver transplantation typically cures HE, but HE does not increase the MELD score, and therefore does not contribute to the likelihood of liver transplantation.

Address: Baylor College of Medicine and Baylor-St. Luke's Medical Center, Division of Abdominal Transplantation, 6620 Main Street #1425, Houston, TX 77030, USA. Electronic address: [email protected].

DOI: 10.1016/j.cld.2015.04.005

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MeSH Terms: Amino Acids, Branched-Chain, Ammonia, Arteriovenous Fistula, Dipeptides, Gastrointestinal Agents, Glycerol, Hepatic Encephalopathy, Humans, Lactulose, Liver Failure, Malnutrition, Ornithine, Phenylbutyrates, Probiotics, Rifamycins, Rifaximin